Tumors in Drosophila and Antibacterial Immunity

Abstract

Melanotic tumors in Drosophila have been the subject of much interest and some controversy since the first strain bearing these hereditary tumors was reported by Bridges in 1916. The tumors consist of aggregates of polygonal and fusiform cells that appear early in life, do not divide, but gradually undergo dissolution and pigmentation as metamorphosis proceeds. They are usually scored by determining the residual melanin in larval, pupal, and imaginal stages (Fig. 1). We collected a large number of strains and studied their behavior in response to various treatments (Burdette, 1951, 1959a; Burdette and Carver, 1970). All those which we examined were benign, and susceptibility was found to be related to multiple genes. Usually there are modifying genes that enhance or suppress respectively the main gene(s). Some of the main genes have been located precisely, and more of the genes for susceptibility are located on the second chromosome than elsewhere. However, one, two, three, or all chromosomes carry these genes in some strains. In a series of interstrain crosses, we found that very few of the genes are alleles (Burdette and Olivier, 1951). Penetrance varies from less than 1 to more than 99%, depending on the strain, temperature, nutrition, and other conditions of culture (Burdette, 1952a 1959a; Herskowitz and Burdette, 1951). Chromosomal aberrations are not obligate for tumors to appear, and we were able to obtain back mutation with x-irradiation in one strain, thus eliminating the possibility that the effect resulted from a small deletion (Burdette, 1959a). No consistent increment or decrement in incidence was obtained when heterochromatin in the form of hyperploid or hypoploid Y chromosomes were varied in tumor strains of Drosophila (Burdette, 1959b).